Bottom Line:
Severe burn injuries may result in gastrointestinal paralysis, and barrier dysfunction due to gut ischemia and lowered vagus excitability.The plasma diamine oxidase (DAO) and intestinal permeability decreased significantly after scald injury in the EA group compared with others.However, EA after atropine injection or cervical vagotomy failed to improve intestinal motility and mucosa blood flow suggesting that the mechanism of EA may be related to the activation of the cholinergic nerve pathway.

ABSTRACTSevere burn injuries may result in gastrointestinal paralysis, and barrier dysfunction due to gut ischemia and lowered vagus excitability. In this study we investigate whether electroacupuncture (EA) at Zusanli (ST36) could prevent severe scalds-induced gut ischemia, paralysis, and barrier dysfunction and whether the protective role of EA at ST36 is related to the vagus nerve. 35% burn area rats were divided into six groups: (a) EAN: EA nonchannel acupoints followed by scald injury; (b) EA: EA at ST36 after scald injury; (c) VGX/EA: vagotomy (VGX) before EA at ST36 and scald injury; (d) VGX/EAN: VGX before EAN and scald injury; (e) atropine/EA: applying atropine before scald injury and then EA at ST36; (f) atropine/EAN: applying atropine before scald injury and then EA at nonchannel acupoints. EA at the Zusanli point significantly promoted the intestinal impelling ratio and increased the amount of mucosal blood flow after scald injury. The plasma diamine oxidase (DAO) and intestinal permeability decreased significantly after scald injury in the EA group compared with others. However, EA after atropine injection or cervical vagotomy failed to improve intestinal motility and mucosa blood flow suggesting that the mechanism of EA may be related to the activation of the cholinergic nerve pathway.

fig1: Intestinal impelling ratio was detected at −0.5, 2, and 6 h after scalds injury. Data are expressed as means ± SD (n = five animals at every time point per group). ∗ versus −0.5 h among the same group, P < 0.05; # versus EA group among 2 h and 6 h, P < 0.05.

Mentions:
Figure 1 illustrates the effect of EA at ST36 on the intestinal impelling ratio after 35% of TBSA scald injury. Scald injury induced gut paralysis and decreased the intestinal impelling ratio. EA at ST36 increased the intestinal impelling ratio after scald injury, while EA at nonchannel acupoints, vagotomy, or intraperitoneal injection of atropine before EA at ST36 reversed its antiparalysis effects. This evidence suggests that EA at ST36 attenuates the decrease of the intestinal impelling ratio after scalds injury.

fig1: Intestinal impelling ratio was detected at −0.5, 2, and 6 h after scalds injury. Data are expressed as means ± SD (n = five animals at every time point per group). ∗ versus −0.5 h among the same group, P < 0.05; # versus EA group among 2 h and 6 h, P < 0.05.

Mentions:
Figure 1 illustrates the effect of EA at ST36 on the intestinal impelling ratio after 35% of TBSA scald injury. Scald injury induced gut paralysis and decreased the intestinal impelling ratio. EA at ST36 increased the intestinal impelling ratio after scald injury, while EA at nonchannel acupoints, vagotomy, or intraperitoneal injection of atropine before EA at ST36 reversed its antiparalysis effects. This evidence suggests that EA at ST36 attenuates the decrease of the intestinal impelling ratio after scalds injury.

Bottom Line:
Severe burn injuries may result in gastrointestinal paralysis, and barrier dysfunction due to gut ischemia and lowered vagus excitability.The plasma diamine oxidase (DAO) and intestinal permeability decreased significantly after scald injury in the EA group compared with others.However, EA after atropine injection or cervical vagotomy failed to improve intestinal motility and mucosa blood flow suggesting that the mechanism of EA may be related to the activation of the cholinergic nerve pathway.

ABSTRACTSevere burn injuries may result in gastrointestinal paralysis, and barrier dysfunction due to gut ischemia and lowered vagus excitability. In this study we investigate whether electroacupuncture (EA) at Zusanli (ST36) could prevent severe scalds-induced gut ischemia, paralysis, and barrier dysfunction and whether the protective role of EA at ST36 is related to the vagus nerve. 35% burn area rats were divided into six groups: (a) EAN: EA nonchannel acupoints followed by scald injury; (b) EA: EA at ST36 after scald injury; (c) VGX/EA: vagotomy (VGX) before EA at ST36 and scald injury; (d) VGX/EAN: VGX before EAN and scald injury; (e) atropine/EA: applying atropine before scald injury and then EA at ST36; (f) atropine/EAN: applying atropine before scald injury and then EA at nonchannel acupoints. EA at the Zusanli point significantly promoted the intestinal impelling ratio and increased the amount of mucosal blood flow after scald injury. The plasma diamine oxidase (DAO) and intestinal permeability decreased significantly after scald injury in the EA group compared with others. However, EA after atropine injection or cervical vagotomy failed to improve intestinal motility and mucosa blood flow suggesting that the mechanism of EA may be related to the activation of the cholinergic nerve pathway.